The aim of the present study was to evaluate the clinical efficacy of platelet-rich fibrin (PRF) in preserving the alveolar ridge following human tooth extraction. A total of 28 patients were divided into two groups: The experimental and control groups (n=14 each). Following tooth extraction, the experimental group was implanted with PRF membrane, whereas the control group was not. The gingival healing effect was assessed at 7 days, 1 and 3 months later. Cone-beam computed tomography was performed immediately and at 3 months following tooth extraction. The changes in alveolar ridge height, width, and bone mineral density were compared between the two groups. The alveolar bone was removed using the ring drill during the implant surgery at 3 months following tooth extraction. Histomorphometric evaluation was performed to compare new bone formation between groups. The patients in the experimental group reportedly felt better compared with the patients in the control group. The healing of gingival tissue was better in the experimental group than in the control group. A significantly greater novel bone area was observed in the PRF group compared with the control group (P<0.01). However, no statistically significant differences were observed in the mean value of buccal alveolar ridge height, lingual/palatal alveolar ridge height and alveolar ridge width between the two groups. These results suggested that PRF was advantageous in human alveolar ridge preservation with ease of use and simple handling. Histological analysis of novel bone formation confirmed that PRF increased the quality of the novel bone and enhanced the rate of bone formation, despite the effect of PRF was not significant to reduce alveolar bone resorption in the extraction socket alone.

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Diphyllin is a natural component of traditional Chinese medicine, which effectively inhibits V-ATPase activity and affects the progression of cancer. However, few studies have been conducted on esophageal cancer, and the mechanisms remain to be elucidated. The present study revealedthat diphyllin inhibited proliferation and induced S arrest in esophageal cancer cell lines TE-1 and ECA-109. Further experiments revealed that diphyllin inhibited V-ATPase activity and decreased the mRNA expression of mammalian target of rapamycin complex 1 (mTORC1), hypoxia-inducible factor-1α (HIF-1α), and vascular endothelial growth factor (VEGF). The present study also revealed that diphyllin inhibited proliferation and reduced the formation of new blood vessels. Diphyllin inhibited blood metastasis by regulating the mTORC1/HIF-1α-/VEGF pathway, therefore it could be considered as a new V-ATPase inhibitor to treat esophageal cancer.